Scar architecture in hypertrophic cardiomyopathy—the geometry of fate

This editorial refers to ‘Scar architecture as a structural biomarker of ventricular arrhythmias and sudden cardiac death in patients with hypertrophic cardiomyopathy: a cardiac magnetic resonance study’ by P. Francia et al., https://doi.org/10.1093/ehjci/jeaf297. In hypertrophic cardiomyopathy, risk is written not only in the mass of scar but in its design. Over the last two decades, late gadolinium enhancement cardiac magnetic resonance (LGE-CMR) has reshaped how we see fibrosis in hypertrophic cardiomyopathy (HCM). What was once an invisible substrate has become a visible predictor of sudden cardiac death (SCD). Yet despite the inclusion of LGE extent into modern risk models, a sense of dissatisfaction remains: why do some patients with modest fibrosis fall victim to ventricular arrhythmias, while others with extensive enhancement remain arrhythmia-free? The study by Francia et al,1 published in this issue of EHJ-Cardiovascular Imaging, brings us a step closer to an answer. It suggests that risk in HCM may depend less on how much scar exists, and more on how that scar is built, its geometry, its corridors, and the silent logic embedded within its structure. The investigators analysed 410 patients with HCM across five European centres who underwent LGE-CMR. Using a dedicated post-processing platform (ADAS-3D), they reconstructed each ventricle in three dimensions, separating core scar, border-zone (BZ) tissue, and the narrow BZ channels that interlace them. These channels, strands of partially viable myocardium insulated within fibrosis, represent the structural pathways for re-entry. The findings are compelling, even as they await prospective validation. Roughly one-third of all patients (and nearly 90% of those with VT/VF events) harboured such channels. Quantitatively, BZ channel mass independently predicted the composite endpoint of sustained VT, VF, or appropriate ICD therapy, even after adjustment for ESC and AHA/ACC guideline-based risk categories. These results are in line with previous studies showing that the presence of channels predicts ICD events in both primary prevention2,3 and secondary prevention,4 CRT,5 and more recently in post-VT ablation patients.6,7 Adding this single architectural parameter significantly improved both discrimination and reclassification, nudging risk assessment towards a substrate-informed future. In simple terms, the geometry of fibrosis, not its quantity, governed fate. At its core, this study recasts fibrosis from a static scar to a living map of vulnerability. The 3D arrangement of border-zone tissue defines the conduction corridors through which re-entry propagates. In ischaemic cardiomyopathy, this concept has been validated histologically and functionally; here, it is extended convincingly to the non-ischaemic terrain of HCM. The HCM myocardium, with its chaotic myofibrillar disarray and interwoven fibrotic strands, is a natural architecture of anisotropy. Within that complexity lie the protected corridors that sustain re-entrant VT, a geometry formed not by coronary occlusion but by sarcomeric genetics and mechanical stress. The observation that small, heterogeneous scars with preserved channel organization can be more arrhythmogenic than large homogeneous scars echoes a deeper principle: in electrophysiology, topology often trumps volume. From a mechanistic perspective, these findings help unify several previously distinct observations. Texture heterogeneity, LGE entropy, and radiomic complexity all hinted at microstructural risk. The concept of scar channels provides the anatomical embodiment of that risk, transforming mathematical texture into spatial substrate. This is the point where imaging meets electrophysiology, where the pixel becomes a pathway. Contemporary SCD prevention in HCM relies on clinical and echocardiographic factors, complemented by LGE burden. These models identify the high-risk extremes but struggle with the large middle ground, patients whose calculated 5-year SCD risk sits in the grey zone between 2% and 6%. It is precisely here that architectural information may yield clinical value. By showing that BZ channel mass refines risk even within guideline-defined low-risk strata, Francia et al. suggest that substrate-based imaging could potentially sharpen ICD decision-making and perhaps spare some patients unnecessary implants. Importantly, the post-processing approach is based on a commercially available platform, lowering the technical barrier for multicentre adoption. Still, translation will require methodologic discipline. As the authors acknowledge, differences in scanner type, PSIR vs. magnitude reconstruction, and segmentation thresholds can subtly alter scar morphology.8 Cross-vendor harmonization, standard reporting of quantitative scar metrics, and disease-specific validation of algorithms in HCM are essential next steps. The recent cross-platform comparisons by Laan and colleagues underscore how such nuances can tilt quantitative outputs, and, by extension, risk predictions.9 Every discipline evolves its own vocabulary. In cardiomyopathy, ‘fibrosis burden’ has been the language of risk. This paper teaches us a richer dialect, one of architecture, channels, and connectivity. It moves the field from a scalar measurement to a structural one, and from a population-based prediction to a patient-specific map. This language also speaks to the broader convergence of imaging, computation, and electrophysiology. As we move toward digital-twin models of the heart, metrics such as BZ channel density will likely serve as part of the geometric inputs for personalized simulations of arrhythmia inducibility.10 The frontier is not merely visualizing scar but understanding how its architecture might govern excitation. In that sense, geometry becomes the bridge between image and impulse. Like all retrospective analyses, this work invites prospective validation. The number of arrhythmic events remains modest, and the algorithm was derived from ischaemic substrates before being repurposed for HCM. Yet the robustness of the findings across risk models and the biological plausibility of the mechanism lend the results credibility, even as they remain hypothesis-generating. Future studies may explore longitudinal remodelling: how do these channels evolve as hypertrophy progresses or regresses with therapy? Serial CMR could help clarify whether the geometry of fate is fixed or dynamic, whether the heart, like any architectural structure, can be remodelled before collapse. The phrase geometry of fate may sound poetic, but here it captures a tangible reality, albeit one that still awaits further validation. The organization of fibrosis, its corridors and boundaries, determines the routes available to electrical waves and, ultimately, to arrhythmia itself. What Francia et al. offer is not only a new biomarker but a new way of seeing: risk as architecture. In hypertrophic cardiomyopathy, every scar is a structure, every channel a potential path to peril. By learning to read these designs, we move one step closer to transforming fate from geometry into knowledge, and knowledge into prevention. Pranav Bhagirath (MD PhD (Conceptualization [lead]; Writing—original draft [lead]; Writing—review & editing [lead])) and Ivo Roca-Luque (MD PhD (Conceptualization [supporting]; Writing—original draft [supporting]; Writing—review & editing [equal])) The data underlying this article will be shared on reasonable request to the corresponding author.